Transcriptome changes following treatment of human cancer cells with actinomycin D, nutlin-3a or camptothecin

Actinomycin D, nutlin-3a and camptothecin are activators of the p53 tumor suppressor protein. These substances induce different posttranslational modifications of p53 and consequently they activate p53 to different degrees. Nutlin-3a appears to be the weakest activator, whereas camptothecin - the strongest. Interestingly, actinomycin D and nutlin-3a, when applied together (A+N), synergize in activation of p53 and consequently, in transcriptional regulation of its target genes. The goal of the project was to find out genes up- or down-regulated by treatment of cells with either actinomycin D, nutlin-3a, A+N or camptothecin in order to identify the new candidate, p53-regulated genes.